New therapeutics that treat rheumatoid arthritis by blocking T-cell activation.

Despite the recent introduction of several new biological products, there remains a significant unmet medical need in rheumatoid arthritis. A focus on the aberrant activation of autoimmune T cells, which is integral to pathogenesis, is a promising approach involved in several of these new therapies. In choosing a molecular target for the modification of T-cell function, it is argued in this article, that within co-stimulatory pathways, CD80 could have a more compelling rationale than CD86. Data are presented showing that CD80-mediated T-cell activation can be inhibited using a small-molecule antagonist, which offers the potential to prevent the inflammatory process leading to joint destruction.